Modeling the encephalopathy of prematurity in animals: the important role of translational research.
Modeling the encephalopathy of prematurity in animals: the important role of translational research.
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DOI：
10.1155/2012/295389
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发表时间：
2012
影响因子：
1.5
通讯作者：
Volpe JJ
中科院分区：
文献类型：
--
作者：
Kinney HC;Volpe JJ
早产儿脑损伤的翻译研究依赖于人类神经病理的描绘，以便动物模型忠实地重申这一点，从而确保与人类状况直接相关。人类早产儿脑损伤的主要底物是早产儿脑病，其特征是灰质和白质病变反映了获得性侮辱、发育轨迹改变和修复现象。在这里，我们重点介绍了人类早产儿脑发育和早产儿脑病的关键特征，这些特征对于动物建模至关重要。在动物模型中完全模拟复杂的人类神经病理学是困难的。许多模型关注与特定功能相关的机制，例如，大脑白质中早髓鞘少突胶质细胞的丢失。然而，同时处理少突胶质细胞、神经元和轴突损伤的动物模型具有破译共同机制和协同治疗以改善早产儿脑病的全球后果的潜力。
Translational research in preterm brain injury depends upon the delineation of the human neuropathology in order that animal models faithfully reiterate it, thereby ensuring direct relevance to the human condition. The major substrate of human preterm brain injury is the encephalopathy of prematurity that is characterized by gray and white matter lesions reflecting combined acquired insults, altered developmental trajectories, and reparative phenomena. Here we highlight the key features of human preterm brain development and the encephalopathy of prematurity that are critical for modeling in animals. The complete mimicry of the complex human neuropathology is difficult in animal models. Many models focus upon mechanisms related to a specific feature, for example, loss of premyelinating oligodendrocytes in the cerebral white matter. Nevertheless, animal models that simultaneously address oligodendrocyte, neuronal, and axonal injury carry the potential to decipher shared mechanisms and synergistic treatments to ameliorate the global consequences of the encephalopathy of prematurity.